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Amyloid beta (Aβ) protofibrils are intermediate, soluble aggregates formed during the self-assembly of amyloid beta peptides, particularly Aβ(1–40) and Aβ(1–42), which are central to the pathology of Alzheimer’s disease. These protofibrils represent a metastable state between smaller oligomers and mature amyloid fibrils. They are considered highly relevant as toxic species in neurodegenerative processes, disrupting cellular membrane integrity by inducing reactive oxygen species generation and lipid peroxidation. Compounds that stabilize or sequester Aβ peptides into non-toxic oligomeric or protofibrillar forms may have therapeutic potential if they prevent engagement with toxic pathways leading to cell damage or death.
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